Abstract
Exercise-induced hypoalgesia is well described, but the underlying mechanisms are unclear. The aim of this study was to examine the effect of exercise on somatosensory evoked potentials, laser evoked potentials, pressure pain thresholds and heat pain thresholds. These were recorded before and after 3-min of isometric elbow flexion exercise at 40% of the participant's maximal voluntary force, or an equivalent period of rest. Exercise-induced hypoalgesia was confirmed in two experiments (Experiment 1–SEPs; Experiment 2–LEPs) by increased pressure pain thresholds at biceps brachii (24.3 and 20.6% increase in Experiment 1 and 2, respectively; both d > 0.84 and p < 0.001) and first dorsal interosseous (18.8 and 21.5% increase in Experiment 1 and 2, respectively; both d > 0.57 and p < 0.001). In contrast, heat pain thresholds were not significantly different after exercise (forearm: 10.8% increase, d = 0.35, p = 0.10; hand: 3.6% increase, d = 0.06, p = 0.74). Contrasting effects of exercise on the amplitude of laser evoked potentials (14.6% decrease, d = −0.42, p = 0.004) and somatosensory evoked potentials (10.9% increase, d = −0.02, p = 1) were also observed, while an equivalent period of rest showed similar habituation (laser evoked potential: 7.3% decrease, d = −0.25, p = 0.14; somatosensory evoked potential: 20.7% decrease, d = −0.32, p = 0.006). The differential response of pressure pain thresholds and heat pain thresholds to exercise is consistent with relative insensitivity of thermal nociception to the acute hypoalgesic effects of exercise. Conflicting effects of exercise on somatosensory evoked potentials and laser evoked potentials were observed. This may reflect non-nociceptive contributions to the somatosensory evoked potential, but could also indicate that peripheral nociceptors contribute to exercise-induced hypoalgesia.
Highlights
Exercise relieves pain for many chronic diseases (Hayden et al, 2005; Busch et al, 2007; Fransen et al, 2015), but the mechanisms are poorly understood
T-tests showed there was a large and significant effect of isometric exercise on increasing Pressure pain thresholds (PPTs) over biceps brachii [Experiment 1: 24.3 ± 17.6% increase, d = 0.84 (0.45–1.3), p < 0.001; Experiment 2: 20.6 ± 8.3% increase, d = 0.99 (0.59–1.49), p < 0.001] and a moderate and significant effect on increasing PPT over first dorsal interosseous [Experiment 1: 18.8 ± 11.6% increase, d = 0.57 (0.28–0.9), p < 0.001; Experiment 2: 21.5 ± 11.1% increase, d = 0.67 (0.42–0.98), p < 0.001], whereas PPTs at both muscles were similar before rest and before exercise
The different behavior of the somatosensory evoked potentials to the laser evoked potentials following exercise could indicate that peripheral nociceptors contribute to exerciseinduced hypoalgesia
Summary
Exercise relieves pain for many chronic diseases (Hayden et al, 2005; Busch et al, 2007; Fransen et al, 2015), but the mechanisms are poorly understood. The well-described phenomenon of exercise-induced hypoalgesia (EIH) (Naugle et al, 2012) suggests that exercise can reduce pain directly via adjustments at some point(s) in the transduction, transmission and processing of noxious stimuli. Animal studies have shown that exercise-induced changes in opioids, cannabinoids, catecholamines, and nitric oxide might all contribute to EIH (Galdino et al, 2010a,b, 2015a,b; de Souza et al, 2013; Fuss et al, 2015), whereas human investigations have yielded more equivocal findings (Janal et al, 1984; Kemppainen et al, 1986, 1990; Droste et al, 1991; Koltyn et al, 2014). Ellingson et al (2014) showed that conditioned pain modulation is likely only a minor contributor to EIH
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